F
Fuyuki Kametani
Researcher at Institute of Medical Science
Publications - 170
Citations - 6514
Fuyuki Kametani is an academic researcher from Institute of Medical Science. The author has contributed to research in topics: Amyloid & Amyloidosis. The author has an hindex of 36, co-authored 157 publications receiving 5076 citations. Previous affiliations of Fuyuki Kametani include Tokyo Metropolitan University & Hiroshima University.
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Journal ArticleDOI
Phosphorylated TDP-43 in frontotemporal lobar degeneration and amyotrophic lateral sclerosis.
Masato Hasegawa,Tetsuaki Arai,Takashi Nonaka,Fuyuki Kametani,Mari Yoshida,Yoshio Hashizume,Thomas G. Beach,Emanuele Buratti,Francisco E. Baralle,Mitsuya Morita,Imaharu Nakano,Tatsuro Oda,Kuniaki Tsuchiya,Haruhiko Akiyama +13 more
TL;DR: The aim of this study was to identify the phosphorylation sites and responsible kinases, and to clarify the pathological significance ofosphorylation of TDP‐43.
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Reconsideration of Amyloid Hypothesis and Tau Hypothesis in Alzheimer's Disease
Fuyuki Kametani,Masato Hasegawa +1 more
TL;DR: Recent findings indicate that the main factor underlying the development and progression of AD is tau, not Aβ, and the deficiencies of the amyloid hypothesis are described.
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Structures of α-synuclein filaments from multiple system atrophy
Manuel Schweighauser,Yang Shi,Airi Tarutani,Airi Tarutani,Fuyuki Kametani,Alexey G. Murzin,Bernardino Ghetti,Tomoyasu Matsubara,Taisuke Tomita,Takashi Ando,Kazuko Hasegawa,Shigeo Murayama,Mari Yoshida,Masato Hasegawa,Sjors H.W. Scheres,Michel Goedert +15 more
TL;DR: Cryo-electron microscopy reveals the structures of α-synuclein filaments from the brains of individuals with multiple system atrophy, which has implications for understanding the mechanisms of aggregate propagation and neurodegeneration in the human brain.
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Longer forms of amyloid beta protein: implications for the mechanism of intramembrane cleavage by gamma-secretase.
Yue Qi-Takahara,Maho Morishima-Kawashima,Yu Tanimura,Georgia Dolios,Naoko Hirotani,Yuko Horikoshi,Fuyuki Kametani,Masahiro Maeda,Takaomi C. Saido,Rong Wang,Yasuo Ihara +10 more
TL;DR: An α-helical model is proposed in which longer Aβ species generated by ϵ-cleavage is cleaved at every three residues in its carboxyl portion in a dose-dependent manner.
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Truncation and pathogenic mutations facilitate the formation of intracellular aggregates of TDP-43
TL;DR: It is proposed that generation and aggregation of phosphorylated C-terminal fragments of TDP-43 play a primary role in the formation of inclusions and resultant loss of normal T DP-43 localization, leading to neuronal degeneration in TDP -43 proteinopathy.